Exam 4 Flashcards
1
Q
F0 Domain
A
- imbedded in the intermembrane
2
Q
Gamma Subunit
A
- In the F1 domain of ATP synthase
- Connected to the C-ring and to the alpha-subunit and beta-subunit of the F1 domain (matrix side)
- Is the driving force of the C-ring rotation
- Influences the conformation of the beta-subunit
- Propelled by the movement of protons
3
Q
Alpha Subunit
A
- Acts as spacers between the beta-subunits
4
Q
Beta Subunit
A
- Can exist in three different conformations
- Open (O) - going to release the ATP and be open for ADP + Pi to enter
- Loose (L) - going to bind ADP + Pi
- Tight (T) - converts ADP + Pi to ATP
5
Q
Respiratory Control
A
- ADP concentration controls rate of O2 consumption
- ATP and ETC are coupled
6
Q
Glycerol-3-Phosphate Shuttle
A
- Predominant in the muscle
- Shuttles FAD and FADH2
- Will yield less ATP than Malate-Aspartate Shuttle because of the use of FAD
7
Q
Malate-Aspartate Shuttle
A
- Predominant in the liver (and heart)
- Uses NADH to accept cytoplasmic electrons
- Conserves NADH and no ATP is lost
8
Q
ATP Synthesis Inhibitors
A
- Inhibition of the ETC at any point (respiratory inhibitors)
- Anything that prevents O2 from accepting e-s
- Direct inhibition of ATP synthase
- This means you are going to have a buildup of ADP, but the ETC will back up as well since the e- carriers are not being re-oxidized
- If you don’t make ATP, then the ETC is not going to keep going, there is a limit for the pmf to be reached
- Disruption of proton gradient against IMM - uncouplers
- ETC keeps going, but protons are coming back into the matrix but not by ATP synthase
- pmf will decrease, driving the ETC, but no ATP will be made
9
Q
Respiratory Inhibitors
A
- Rotenone (pesticide), Amytal (barbituate)
- Block at Complex I
- The e- from NADH will not reach CoQ and therefore NADH will build up and negatively modify ETC
- Antimycin (anti-fungal)
- Block at Complex III
- CoQ cannot deliver to Complex III and previous carriers will build up
- Cyanide, Azide, CO
- Target Complex IV
- Cyanide and Azide keep iron in the oxidized, Fe3+ form
- CO binds to Fe2+ so there is no back and forth redox reaction to be able to deliver those e- to O2
10
Q
ATP Synthase Inhibitors
A
- Oligomycin
- Will attack F0 domain
- DCCD
11
Q
Uncouplers
A
- Separate the tight coupling between ETC and oxidative phosphorylation (ATP synthesis)
- Can be chemical or physiological
- Chemical has no regulation, physiological does
- Will keep consuming O2 and ETC will still run, to maintain pmf/proton gradient, but no ATP will be produced
- Have an aromatic ring that allows it to interact with the inner membrane (different method of transportation for the protons across the membrane)
- Physiological uncoupler: UCP-1
12
Q
Glycogen
A
- Polymer of glucose
- Primarily stored in the liver and the skeletal muscle
13
Q
Polysaccharides
A
- All are made up of glucose
- Cellulose - beta-1,4 linkage; primarily for structural support
- Starch - primarily for energy storage
- Glycogen - alpha-1,4 and alpha-1,6 linkage; branched
- Amylopectin - alpha-1,4 and alpha-1,6 linkage; branched
- Amylose - linear structure
14
Q
Glycogen Synthase
A
- major enzyme, that is going to catalyze the alpha-1,4 linkage
15
Q
Glycogenin
A
- Makes primer for glycogen synthesis
- Can synthesize the primer de novo, but do not necessarily degrade the primer, so not always needed
16
Q
Fatty Acid Synthesis
A
- Major site is in the liver, not the adipose tissue
- If insulin is present, then acetyl CoA will go into fatty acid synthesis
- Acetyl CoA is the starting substrate
- Occurs in the cytoplasm
- NADPH is needed, not NADH because glyocolysis and fatty acid synthesis need to be able to take place at the same time and both happen in the cytoplasm
17
Q
Protein Phosphatase 1 (PP1)
A
- Activated by the fed state, high I/G ratio
- Dephosphorylates inactive gylcogen synthase and glycogen phosphorylase
18
Q
Glycogen Synthase Kinase
A
- Deactivated in the fed state, high I/G ratio, but a protein kinase
- Deactivation of glycogen synthase kinase allows glycogen synthase to remain dephosphorylated and active
19
Q
Inactive Glycogen Synthase
A
- Dephosphorylated by PP1
- Dephosphorylation of inactive glycogen synthase makes it become active
20
Q
Glycogen Phosphorylase
A
- Dephosphorylated by PP1
- Becomes inactive, so the new glycogen produced is not degraded
21
Q
NADPH
A
- Reducing equivalent needed for fatty acid synthesis
- Generated from two sources:
- Malic enzyme, that converts malate into pyruvate
- Pentose-P Pathway
22
Q
Acetyl CoA Carboxylase (ACC)
A
- Adds a CO2 to acetyl CoA to produce malonyl CoA
- Biotin is required as a co-enzyme for the production of malonyl CoA
- Activation and rate limiting step in fatty aid synthesis
23
Q
Regulation of Acetyl CoA Carboxylase (ACC)
A
- AMPK (AMP dependent protein kinase )- activated by AMP and is going to be inhibited by ATP; more active in the fasted state
- Protein Phosphatase 2A (PP2A)
- Stimulated by insulin
- Citrate
- Allosterically modified
- Can bind to the phosphorylated, less active form of the enzyme, so it can activate the enzyme, but not 100%
- Allows fatty acid synthesis to get started before dephosphorylating cascade finishes
- Palmotyl CoA
- Final product of fatty acid synthesis, and will allosterically modify ACC
24
Q
Glycerol Kinase
A
- Only found in the liver, not adipose tissue
- Glycerol can be recycled from the break down of triglycerides
- Glycerol concentration does not strictly rely on glycolysis
25
Q
Phosphatidate
A
- Common intermediate for phospholipids and triglycerides
- Has its phosphate removed to produce DAG and a third fatty acid is added to create triaglycerol
26
Q
Chylomicron
A
- Made in the small intestine
- Transports dietary triglycerides
- Become remnants when triglycerides are unloaded
27
Q
Very Low Density Lipid (VLDL)
A
- Made in the liver
- Transports newly synthesized triglycerides
- Becomes IDL and eventually LDL after triglycerides are unloaded
